Search Results (81)

Chronic coronary syndrome (CCS) and atrial fibrillation (AF) are prevalent cardiovascular conditions that share numerous risk factors and pathophysiological mechanisms. While clinical scores commonly used in AF—such as CHA₂DS₂VA (which includes congestive heart failure, hypertension, age ≥ 75, diabetes, stroke/TIA, vascular disease, and age 65–74), HAS-BLED (which incorporates hypertension, abnormal renal/liver function, stroke, bleeding history, labile INR, elderly age, and drug/alcohol use), and C₂HEST (incorporating coronary artery disease, COPD, hypertension, elderly age ≥ 75, systolic heart failure, and thyroid disease)—are traditionally applied to rhythm or bleeding risk prediction, their value in estimating the angiographic severity of coronary artery disease (CAD) remains underexplored. We conducted a prospective, single-center study including 131 patients with suspected stable CAD referred for coronary angiography, stratified according to coronary angiographic findings into two groups: significant coronary stenosis (S-CCS) and non-significant coronary stenosis (N-CCS). At admission, AF-related scores (CHA₂DS₂, CHA₂DS₂VA, CHA₂DS₂VA-HSF, CHA₂DS₂VA-RAF, CHA₂DS₂VA-LAF, HAS-BLED, C₂HEST, and HATCH) were calculated. CAD severity was subsequently assessed using the SYNTAX and Gensini scores. Statistical comparisons and Pearson correlation analyses were performed to evaluate the association between clinical risk scores and angiographic findings. Patients in the S-CCS group had significantly higher scores in CHA₂DS₂VA (4.09 ± 1.656 vs. 3.20 ± 1.338, p = 0.002), HAS-BLED (1.98 ± 0.760 vs. 1.36 ± 0.835, p < 0.001), CHA₂DS₂VA-HSF (6.00 ± 1.854 vs. 5.26 ± 1.712, p = 0.021), and C₂HEST (3.49 ± 1.501 vs. 2.55 ± 1.279, p < 0.001). Multivariate logistic regression identified HAS-BLED and C₂HEST as independent predictors of significant coronary lesions. A threshold value of HAS-BLED ≥ 1.5 and C₂HEST ≥ 3.5 demonstrated moderate discriminative ability (AUC = 0.694 and 0.682, respectively), with acceptable sensitivity and specificity. These scores also demonstrated moderate to strong correlations with both Gensini and SYNTAX scores. AF-related clinical scores, especially HAS-BLED and C₂HEST, may serve as practical and accessible tools for early CAD risk stratification in patients with suspected CCS. Their application in clinical practice may serve as supplementary triage tools to help prioritize patients for further diagnostic evaluation, but they are not intended to replace standard imaging or testing. Full article

As the population of adults with congenital heart disease (ACHD) continues to grow, a significant and often underrecognized complication is the development of cardiorenal syndrome (CRS)—a complex, bidirectional interaction between cardiac and renal dysfunction. While CRS has been extensively studied in acquired heart failure, its manifestations and implications in ACHD remain insufficiently understood. Emerging data suggest that renal dysfunction is highly prevalent in ACHD, with significant associations to adverse outcomes regardless of cardiac lesion type or functional status. This review explores CRS within three key physiologic categories in ACHD: patients with a systemic right ventricle, those with a subpulmonary right ventricle, and those with Fontan circulation. Each subgroup presents unique hemodynamic challenges that affect renal perfusion, filtration pressure, and systemic congestion, contributing to both acute and chronic renal impairment. The utility of renal biomarkers such as albuminuria, cystatin C, and estimated glomerular filtration rate (eGFR) is emphasized, alongside the importance of early detection and multidisciplinary management. Heart failure therapy tailored to congenital anatomy, neurohormonal modulation, and careful volume control remain the cornerstones of treatment, while transplantation strategies must consider the potential for irreversible end-organ damage. Given the profound implications of CRS on quality of life and survival, a comprehensive understanding of its pathophysiology and management in ACHD is critical to optimizing long-term outcomes in this increasingly complex patient population. Full article

Systemic lupus erythematosus (SLE) is a pleiotropic disease that can present in numerous forms, ranging from mild mucocutaneous symptoms to severe manifestations affecting multiple organs. SLE has the potential to impact any segment of the respiratory system, exhibiting a range of severity levels throughout the different stages of the disease. Pulmonary manifestations in SLE patients can be classified as primary (i.e., directly related to SLE and to immune-mediated damage), secondary to other SLE manifestations (e.g., nephrotic syndrome, renal failure, congestive heart failure), and comorbidities (e.g., infections, cancers, overlapping primary respiratory diseases). Understanding and correctly managing lung involvement in SLE is crucial because pulmonary complications are common and can significantly impact morbidity and mortality in affected patients. Early recognition and appropriate treatment can prevent irreversible lung damage, improve quality of life, and reduce the risk of life-threatening complications. Treatment algorithms are based on the suppression of inflammation, with or without the need for dedicated, supportive care. According to disease severity, available treatments include nonsteroidal anti-inflammatory drugs, corticosteroids, immunosuppressants, and biological agents. In this review, we aim to summarize the current knowledge on lung involvement in SLE and then focus on the management and treatment approaches available for the different forms. Full article

Background/Objectives: Carbohydrate antigen 125 (CA125) is a glycoprotein commonly overexpressed in epithelial ovarian cancer and widely recognized as a tumor marker. However, elevated CA125 levels are also observed in various non-malignant conditions, including diseases affecting mucosal surfaces, pleural or peritoneal effusions, cirrhosis (with or without ascites), endometriosis, uterine fibroids, adenomyosis, pelvic inflammatory disease, and pregnancy. This review aims to explore the role of CA125 in non-malignant serous effusions, highlighting its diagnostic and prognostic potential beyond the realm of oncology. Methods: A comprehensive literature search was conducted across multiple databases and clinical trial registries. Eligible studies included full-text original research articles, reviews, and case reports published in English over the past 10 years. Inclusion criteria were limited to studies involving human subjects and focused on the role of CA125 in non-malignant serous effusions. Results: CA125 is produced by coelomic epithelial cells lining the ovary, pleura, pericardium, and peritoneum. Its serum concentration is not significantly influenced by age, body weight, or renal function, even in the advanced stages of the disease. In peritoneal conditions, CA125 is synthesized by mesothelial cells and serves as a potential marker of peritoneal involvement. The prevailing pathophysiological mechanism suggests that mechanical stretching of mesothelial cells due to ascitic pressure stimulates CA125 release. Similarly, in heart failure, mesothelial cells of the pericardium produce CA125, which correlates with congestion severity, supports risk stratification, and may inform diuretic therapy. Conclusions: While a threshold of 35 U/mL is established for malignancy, no standardized cutoff exists for CA125 in non-malignant conditions. The utility of CA125 measurement in peritoneal, pleural, or pericardial effusions—and cardiovascular diseases such as acute heart failure—for purposes of differential diagnosis, treatment guidance, or prognostication warrants further investigation through prospective clinical trials. Full article

Background: Serum uric acid and serum creatinine ratio (SUA/sCr) is strongly linked to increased cardiovascular risk. Atherosclerotic renal artery stenosis (ARAS) is a secondary cause of hypertension and is associated with ischemic nephropathy, congestive heart failure, accelerated cardiovascular disease, and autonomic dysfunction. The aim of this study was to investigate whether SUA levels and SUA/sCr could represent markers of autonomic dysfunction and increased left ventricular mass index (LVMI) in patients with ARAS. Methods: Patients diagnosed with ARAS were enrolled in the study. All patients underwent clinical evaluation, biochemical analysis, 24 h electrocardiogram (ECG), and Renal Doppler Ultrasound with renal resistive index parameters. Heart rate variability for global autonomic dysfunction was assessed through the analysis of a 24 h ECG to detect the standard deviation of normal-to-normal RR intervals (SDNN). Echocardiographic measurement of LVMI was performed. Results: A total of 27 patients (F = 16 (59%), median age 67 years (IQR 60–77)) diagnosed with ARAS were enrolled in the study. We found a statistically significant negative linear correlation between SUA/sCr and SDNN (r = −0.519, p < 0.01). We found a statistically significant positive linear correlation between SUA/sCr and LVMI (r = 0.413, p < 0.05). Median SDNN was significantly lower in patients with SUA ≥ 5.6 mg/dL than in patients with SUA < 5.6 mg/dL (94.2 (IQR 86.8–108.1) vs. 112.8 (IQR 108.9–114.7), p < 0.01). Median LVMI was significantly higher in patients with SUA ≥ 5.6 mg/dL compared to patients with SUA < 5.6 mg/dL (133 g/m² (IQR 120–149) vs. 111 g/m² (IQR 99–129), p < 0.05). Conclusion: In patients with ARAS, SUA/sCr is associated with autonomic dysfunction and LVMI in ARAS patients. The ratio and related cut-off value of SUA/sCr could represent a useful biomarker to evaluate cardiovascular risk in ARAS patients. Full article

Background: Heart failure (HF), chronic kidney disease (CKD), and atrial fibrillation (AF) frequently coexist, forming a high-risk triad that amplifies morbidity and mortality through shared pathophysiological mechanisms such as neurohormonal activation, fluid overload, and inflammation. Current risk stratification tools, including CHA₂DS₂-VASc and HAS-BLED, inadequately capture the complexity of these multimorbid patients. This study aims to explore the influence of comorbidities, hypertension severity, anticoagulation strategy, and risk scores on hospitalization outcomes in patients with coexisting HF, CKD, and AF. Materials and Methods: A retrospective case study was conducted on 174 hospitalized patients with HF, CKD, and AF. Clinical data included hypertension grade, HF phenotype (HFpEF vs. HFrEF), NYHA classification, renal function (KDIGO stage), stroke and bleeding risk scores (CHA₂DS₂-VASc: congestive heart failure, hypertension, age ≥ 75, diabetes, and stroke/TIA; HAS-BLED: hypertension, abnormal renal/liver function, stroke, bleeding, labile INR, elderly, and drugs/alcohol), comorbidities (neurological, psychiatric, COPD, and diabetes), anticoagulation type (DOACs vs. VKAs), and length of hospital stay. Statistical analysis included Spearman correlation, independent t-tests, and multivariate regression to evaluate associations between variables and clinical outcomes. Results: Most patients were elderly (mean age 75 ± 12), with advanced CKD (stage 3b) and systolic HF (77% HFrEF). Mean CHA₂DS₂-VASc was 5.67, HAS-BLED was 4.40, and ATRIA was 4.74, indicating high stroke and bleeding risk. Anticoagulation was predominantly via DOACs (69.5%). Hypertension severity did not significantly correlate with NYHA class (ρ = −0.14, p = 0.068). Neurological, psychiatric, and metabolic comorbidities showed no significant associations with HF severity. COPD and diabetes correlated inversely with CHA₂DS₂-VASc scores (ρ = −0.83, p = 0.014). No significant differences were observed in hospital stay between HF phenotypes or prior stroke history. In-hospital mortality was low (2.3%). Conclusions: Traditional risk scores do not fully capture the complexity of multimorbid patients. Metabolic comorbidities showed an inverse correlation with stroke risk scores, and no significant correlation was observed between hypertension severity and HF symptom burden. Hypertension and common comorbidities did not correlate with HF symptom burden, and metabolic diseases may paradoxically associate with lower stroke risk scores. These findings highlight the need for improved multimodal risk assessment strategies that consider the heterogeneity of multimorbid populations. Personalized, integrated approaches are essential to optimize anticoagulation, reduce hospitalization, and improve prognosis. Full article

Congestion represents a defining hallmark of heart failure (HF) leading to increased morbidity and mortality in HF patients. While it was traditionally viewed as a simple and uniform state of volume overload, contemporary understanding has emphasized its complexity, distinguishing between intravascular, interstitial, and tissue congestion. Congestion contributes to overt clinical manifestation of HF. However, subclinical congestion often goes undetected, increasing the risk of adverse outcomes. Residual congestion, in particular, remains a frequent and challenging issue, with its persistence at discharge being strongly linked to rehospitalization and poor prognosis. Clinical evaluation often fails to reliably identify the resolution of congestion, highlighting the need for supplementary diagnostic methods. Improvement in imaging modalities, including lung ultrasound, venous Doppler, and echocardiography, have significantly enhanced the detection of congestion. Moreover, biomarkers such as natriuretic peptides, bioactive adrenomedullin, soluble CD146, and carbohydrate antigen 125 offer valuable, complementary insights into fluid distribution and the severity of HF congestion. Therefore, a comprehensive, multimodal strategy that integrates clinical evaluation with imaging and biomarker data is crucial for optimizing the management of congestion in HF. Future approaches should prioritize personalized decongestive therapy, addressing both intravascular and tissue congestion, while aiming to preserve renal function and limit neurohormonal activation. Refinement of these strategies holds promise for improving long-term outcomes, reducing rehospitalizations, and enhancing overall patient prognosis. Full article

Background: The one-year mortality risk for elderly patients undergoing proximal femur fracture repair surgery is three to four times higher compared to the general population. Other than time to surgery, risk factors for postoperative morbidity and mortality following surgery are poorly understood in the elderly. We sought to identify risk factors associated with morbidity and mortality in geriatric patients by anticoagulation status undergoing hip fracture repair. Methods: Patients aged ≥65 years undergoing surgery for hip fracture repair were included (2009–2019) from a US-based hip fracture registry. Factors associated with 90-day mortality were determined using multivariable logistic regression and stratified by antithrombotic agent medication use prior to surgery. Direct oral anticoagulation (DOAC) medications were the largest group, and all antithrombotic agents were included in the delineation. Results: A total of 35,463 patients were identified, and 87.1% (N = 30,902) were DOAC-naïve. Risk factors for 90-day mortality in DOAC-naïve patients were an American Society of Anesthesiologist’s (ASA) classification ≥3 (odds ratio [OR] = 2.56, 95% confidence interval [CI] = 2.24–2.93), preoperative myocardial infarction (OR = 1.87, 95% CI = 1.33–2.64), male gender (OR = 1.73, 95% CI = 1.59–1.88), congestive heart failure (CHF) (OR = 1.64, 95% CI = 1.50–1.80), psychoses (OR = 1.27, 95% CI = 1.15–1.42), renal failure (OR = 1.29, 95% CI = 1.19–1.40), smoking history (OR = 1.19, 95% CI = 1.09–1.29), chronic pulmonary disease (OR = 1.14, 95% CI = 1.05–1.25), increasing age (OR = 1.07, 95% CI = 1.06–1.07), and decreasing body mass index (BMI) (OR = 1.06, 95% CI = 1.05–1.08). Identified factors for mortality in the DOAC group also included ASA classification ≥3 (OR = 2.15, 95% CI = 1.44–3.20), male gender (OR = 1.68, 95% CI = 1.41–2.01), CHF (OR = 1.45, 95% CI = 1.22–1.73), chronic pulmonary disease (OR = 1.34, 95% CI = 1.12–1.61), decreasing BMI (OR = 1.04, 95% CI = 1.02–1.06), and increasing age (OR = 1.02, 95% CI = 1.01–1.03). Conclusions: Regardless of preoperative DOAC status, ASA classification, gender, CHF, chronic pulmonary disease, lower BMI, and higher age are associated with an increased risk of mortality. Some of these comorbidities can be utilized for risk stratification prior to surgery. Full article

Congestion is a key clinical feature of heart failure (HF), contributing to hospitalizations, disease progression, and poor outcomes. While traditionally considered a hemodynamic issue, congestion is now recognized as a systemic process affecting multiple organs. Renal dysfunction arises from impaired perfusion and sodium retention, leading to maladaptive left ventricular remodeling. Hepatic congestion contributes to cholestatic liver injury, while metabolic disturbances drive anemia, muscle wasting, and systemic inflammation. Additionally, congestion disrupts the intestinal barrier and immune function, exacerbating HF progression. Given its widespread impact, effective congestion management requires a shift from a cardiovascular-centered approach to a comprehensive, multidisciplinary strategy. Targeted decongestive therapy, metabolic and nutritional optimization, and immune modulation are crucial in mitigating congestion-related organ dysfunction. Early recognition and intervention are essential to slow disease progression, preserve functional capacity, and improve survival. Addressing HF congestion through personalized, evidence-based strategies is vital for optimizing long-term care and advancing treatment paradigms. Full article

The renal resistive index (RRI), a Doppler ultrasound-derived parameter measuring renal vascular resistance, has emerged as a promising non-invasive tool to evaluate renal hemodynamics in critically ill patients, particularly those with acute respiratory distress syndrome (ARDS) and heart failure (HF). This narrative review examines the current evidence for RRI measurement in these conditions, exploring its physiological bases, methodology, clinical applications, and limitations. In ARDS, RRI reflects the complex interactions between positive pressure ventilation, hypoxemia, and systemic inflammation, showing a role in predicting acute kidney injury and monitoring response to interventions. In HF, RRI is able to assess venous congestion and cardiorenal interactions and can also serve as a prognostic indicator. Many studies have shown RRI’s superiority or complementarity to traditional biomarkers in predicting renal dysfunction, although its interpretation requires consideration of multiple patient-related factors. Key challenges include operator dependency, lack of standardization, and complex interpretation in multi-organ dysfunction. Future research should focus on measurement standardization, development of automated techniques, investigation of novel applications like intraparenchymal renal resistive index variation, and validation of RRI-guided management strategies. Despite its limitations, RRI represents a valuable tool that offers bedside and real-time insights into renal hemodynamics and potential guidance for therapeutic interventions. Further research is needed to fully clarify its clinical potential and address current limitations, particularly in critical care settings involving multiple organ dysfunction. Full article

Background/Objectives: Left ventricular diastolic dysfunction (LVDD) is associated with unfavorable outcomes, and though it is recognized as an important clinical diagnosis, specific quantification and effective management continue to challenge clinicians, representing an unmet need in modern cardiology. Advanced LVDD diagnosis is likely to have a prognostic role among hospitalized patients. The aim of this study was to describe the prevalence and predictors of advanced LVDD among hospitalized patients and its long-term (5-year) prognostic significance on all-cause mortality. Methods: This was a retrospective observational study of consecutive, non-selected hospitalized patients referred for echocardiography at a tertiary care medical center from October 2013 to February 2024. Diastolic function was classified into normal/LVDD grade I vs. advanced LVDD (grades II and III). Results: A total of 5926 participants were included in the analysis, of whom 3229 (54%) were men, with a mean age of 66 ± 2 years. These included 4779 (81%) patients with normal/LVDD grade I and 1147 (19%) with advanced LVDD. Compared to patients with normal/LVDD grade I, those with advanced LVDD were older, were more likely to be men, and had a higher burden of hypertension, diabetes mellitus, congestive heart failure, atrial fibrillation/flutter and renal failure, abnormal laboratory findings, worse echocardiogram parameters, and longer hospital stay. Multivariate analysis revealed that advanced LVDD was independently associated with increasing age, the male sex, significant aortic stenosis, hypertension, and atrial fibrillation. Patients with advanced LVDD vs. normal/LVDD grade I had higher 5-year all-cause mortality rates (p_log-rank < 0.001). Multivariate Cox proportional hazards regression model revealed that advanced LVDD was associated with a 24% increase in the 5-year mortality rate (HR = 1.236, 95% CI of 1.008–1.517, p = 0.042). Conclusions: Among hospitalized patients referred for echocardiography, the prevalence of advanced LVDD was 19%, and it was independently associated with age, the male sex and the presence of multiple comorbidities. Moreover, advanced LVDD was identified as an independent predictor of long-term all-cause mortality. Advanced LVDD should be proactively diagnosed among admitted patients at risk for early therapy tailoring. Full article

Point-of-care ultrasound (POCUS) has increasingly become an integral part of clinical practice, particularly in nephrology, where its use extends beyond renal assessment to include multi-organ evaluations. Despite challenges such as limited ultrasound training and equipment access, especially in low- and middle-income countries, the adoption of POCUS is steadily rising. This narrative review explores the growing role of multi-organ POCUS in nephrology, with applications ranging from the assessment of congestion phenotypes, cardiorenal syndrome, and hemodynamic acute kidney injury (AKI) to the evaluation of arteriovenous fistulas and electrolyte disorders. In nephrology, POCUS enhances clinical decision making by enabling rapid, bedside evaluations of fluid status, cardiac function, and arteriovenous access. Studies have demonstrated its utility in diagnosing and managing complications such as heart failure, cirrhosis, and volume overload in end-stage renal disease. Additionally, POCUS has proven valuable in assessing hemodynamic alterations that contribute to AKI, particularly in patients with heart failure, cirrhosis, and systemic congestion. This review highlights how integrating ultrasound techniques, including lung ultrasound, venous Doppler, and focused cardiac ultrasound, can guide fluid management and improve patient outcomes. With advancements in ultrasound technology, particularly affordable handheld devices, and the expansion of targeted training programs, the potential for POCUS to become a global standard tool in nephrology continues to grow, enabling improved care in diverse clinical settings. Full article

Background: Pregnant women with congenital heart disease carry a high risk of complications, especially when cardiac function is suboptimal. Increasing evidence suggests that impaired right ventricular (RV) function has a negative effect on placental function, possibly through venous congestion. We report a case series of hepatic and renal venous flow patterns in pregnant women with right ventricular dysfunction after repaired Tetralogy of Fallot (ToF), relative to those observed in normal pregnancy and preeclampsia. Methods: At 20–24 weeks pregnancy, RV function was measured by echocardiography and by cardiovascular magnetic resonance in women with repaired ToF. Combined Doppler-ECG of the hepatic and renal interlobular veins were performed in three women with asymptomatic right ventricular dysfunction. Venous impedance index and pulse transit time were measured and classified as abnormal at >75th and <25th reference percentile, respectively. Results: All three women showed dilated RV and mildly impaired RV function. Both hepatic and intrarenal Doppler flow waves were abnormal and very much resembled the patterns seen in preeclampsia. One of the three women had complications including ventricular tachycardia, intrauterine growth restriction, antenatal bleeding, emergency cesarean section and acute heart failure 2 days postpartum. Conclusions: Pregnant women with mild right ventricular dysfunction after repaired ToF show abnormal venous Doppler flow waves in the liver and kidneys, similar to those observed in preeclampsia. These findings are in line with reported observations on the association between impaired RV function, abnormal return of venous blood, venous congestion and organ dysfunction. The parallel with venous Doppler flow observations in preeclampsia suggest that the venous compartment might play an important role in the etiology of preeclampsia-induced organ dysfunction. Whether this phenomenon directly affects the uteroplacental circulation is to be assessed in future research. Full article

Background: Cardio-renal syndrome (CRS) is a complex condition involving bidirectional dysfunction of the heart and kidneys, in which the failure of one organ exacerbates failure in the other. Traditional pharmacologic treatments are often insufficient to manage the hemodynamic and neurohormonal abnormalities underlying CRS, especially in cases resistant to standard therapies. Device-based therapies have emerged as a promising adjunct or alternative approach, offering targeted intervention to relieve congestion, improve renal perfusion, and modulate hemodynamics. This study aimed to evaluate the efficacy and safety of various device-based therapies in CRS management, utilizing DRI2P2S classification to categorize interventions as dilators, reducers, interstitial modulators, pullers, pushers, and shifters. Methods: A comprehensive analysis of clinical trial data and observational studies involving device-based therapies in patients with CRS was conducted, with a focus on hemodynamic endpoints, renal and cardiac function, symptom relief, and adverse events. Devices included in the analysis were splanchnic denervation systems (dilators), devices for central and pulmonary pressure reduction (reducers), and systems targeting interstitial fluid (fluid shifters), among others. A systematic literature review from 2004 to 2024 was performed using databases including PubMed, Embase, and ClinicalTrials.gov, following PRISMA guidelines for study selection. Data were extracted on patient demographics, device type, trial design, outcomes, and follow-up duration. Results: Device-based therapies demonstrated varying levels of efficacy in CRS, with significant improvements observed in specific parameters. Notable results were a reduction in central venous pressure and improved diuretic responsiveness in acute CRS cases, while also stabilizing or improving renal function. Other relevant endpoints were fewer heart failure hospitalizations and a reduction in renal adverse events, reduced tissue congestion and improved quality of life scores. However, some devices presented challenges, including procedure-related complications and a learning curve for optimal device implantation. Conclusions: Device-based therapies offer a valuable addition to the CRS treatment paradigm, particularly in cases unresponsive to conventional diuretics and other pharmacologic measures. Each of them addresses specific pathophysiological components of CRS and shows promise in improving clinical outcomes. Nevertheless, further large-scale, long-term trials with comprehensive endpoints are needed to establish these therapies’ roles in standard care and to optimize patient selection criteria. Enhanced understanding of device mechanisms and refinement of trial endpoints will be key to maximizing the impact of these therapies on quality of life and clinical outcomes for CRS patients. Full article

Heart failure (HF) is a complex clinical syndrome characterized by the heart’s inability to maintain sufficient circulation, leading to inadequate organ perfusion and fluid buildup. A thorough understanding of the molecular, biochemical, and hemodynamic interactions that underlie this condition is essential for improving its management and enhancing patient outcomes. Recent advancements in cardiovascular research have emphasized the critical role of microRNAs (miRNAs) as post-transcriptional regulators of gene expression, playing an important part in the development and progression of HF. This review aims to explore the contributions of miRNAs, systemic congestion markers, and traditional biomarkers to the pathophysiology of heart failure, with the objective of clarifying their prognostic value and potential clinical applications. Among the miRNAs studied, miR-30d, miR-126-3p, and miR-483-3p have been identified as key players in processes such as left ventricular remodeling, regulation of pulmonary artery pressure, and adaptation of the right ventricle. These findings underscore the importance of miRNAs in modulating the structural and functional changes seen in HF. Beyond the heart, HF affects multiple organ systems, including the kidneys and liver, with markers of dysfunction in these organs—such as worsening renal function and liver stiffness—being closely linked to increased morbidity and mortality. This highlights the interdependence of the heart and other organs, where systemic congestion, indicated by elevated venous pressures, exacerbates organ dysfunction. In this context, traditional biomarkers like natriuretic peptides and cardiac troponins remain vital tools in the diagnosis and management of HF. Natriuretic peptides reflect ventricular strain, while troponins are indicators of myocardial injury, both of which are critical for risk stratification and monitoring disease progression. Emerging diagnostic techniques, such as lung ultrasonography and advanced echocardiographic methods, offer new ways to assess hemodynamic status, further aiding therapeutic decision-making. These techniques, alongside established biomarkers, provide a more comprehensive approach to understanding the complexities of heart failure and managing its impact on patients. In conclusion, miRNAs, systemic congestion markers, and traditional biomarkers are indispensable for understanding HF pathophysiology and determining patient prognosis. The integration of novel diagnostic tools with existing biomarkers holds the promise of improved strategies for the management of heart failure. However, further research is needed to validate their prognostic value and refine their role in optimizing treatment outcomes. Full article